Molecular Carcinogenesis and Chemoprevention Division, Department of Medical Elementology and Toxicology, Faculty of Science, Jamia Hamdard-Hamdard University, Hamdard Nagar, New Delhi, India.
J Pharm Pharmacol. 2012 Jun;64(6):872-81. doi: 10.1111/j.2042-7158.2012.01470.x. Epub 2012 Mar 22.
Cisplatin-induced nephrotoxicity is the main cause for its dose-limited use in the treatment of various cancers and results in acute renal cell injury through generation of reactive oxygen species. Chrysin possess antioxidant, anti-inflammatory and anti-cancer properties. The aim of this study was to investigate the protective efficacy of chrysin against cisplatin-induced nephrotoxicity.
Thirty male Wistar rats were divided into five groups with six rats in each group. Group I served as control and received corn oil (vehicle of chrysin) for 14 days and 0.9% saline (vehicle of cisplatin) on day 14 only. Group II received a single intraperitoneal injection of cisplatin on day 14. Group III and IV were pretreated with two different doses of chrysin in addition to cisplatin and group V received chrysin only. Rats were examined for the effect of chrysin on cisplatin induced depletion of antioxidant enzymes, induction of lipid peroxidation and DNA damage in the kidney, utilizing a well-established model of cisplatin-induced nephropathy.
Pretreatment with chrysin significantly attenuated cisplatin-induced renal oxidative damage by diminishing the DNA damage and toxicity markers, such as creatinine and blood urea nitrogen, lipid peroxidation and xanthine oxidase activity, accompanied by increase in enzymatic (catalase, glutathione peroxidase, glutathione reductase and glutathione-S-transferase) and non-enzymatic (reduced glutathione) antioxidant status. Histological findings further substantiated the protective efficacy of chrysin, which reduced cisplatin-induced renal damage.
The data of the present study suggest that chrysin effectively suppress cisplatin-induced renal injury by ameliorating oxidative stress.
顺铂诱导的肾毒性是其在治疗各种癌症时剂量受限的主要原因，通过产生活性氧导致急性肾细胞损伤。白杨素具有抗氧化、抗炎和抗癌特性。本研究旨在探讨白杨素对顺铂诱导的肾毒性的保护作用。
将 30 只雄性 Wistar 大鼠分为 5 组，每组 6 只。第 1 组作为对照组，在第 14 天接受玉米油（白杨素的载体），仅在第 14 天接受 0.9%生理盐水（顺铂的载体）。第 2 组在第 14 天接受单次腹腔注射顺铂。第 3 组和第 4 组在给予顺铂的同时给予两种不同剂量的白杨素预处理，第 5 组仅给予白杨素。利用建立良好的顺铂诱导肾病模型，研究白杨素对顺铂诱导的抗氧化酶耗竭、脂质过氧化和肾脏 DNA 损伤的影响。
白杨素预处理通过减少 DNA 损伤和毒性标志物（如肌酐和血尿素氮）、脂质过氧化和黄嘌呤氧化酶活性，同时增加酶（过氧化氢酶、谷胱甘肽过氧化物酶、谷胱甘肽还原酶和谷胱甘肽-S-转移酶）和非酶（还原型谷胱甘肽）抗氧化状态，显著减轻顺铂引起的肾氧化损伤。组织学发现进一步证实了白杨素的保护作用，减轻了顺铂引起的肾损伤。
本研究数据表明，白杨素通过改善氧化应激有效抑制顺铂诱导的肾损伤。
